Value of speckle-tracking echocardiography changes in monitoring myocardial dysfunction during treatment of sepsis: potential prognostic implications.

Speckle-tracking echocardiography (STE) has been increasingly used for detection of sepsis-related myocardial dysfunction. However, the impact of strain changes during sepsis treatment has not been defined. This study assessed STE at admission and during the treatment of patients with sepsis to evaluate its changes as a potential factor for predicting in-hospital outcome. This study included 26 patients with sepsis who underwent STE echocardiography on day 1 and 7 during treatment. Myocardial deformation of both ventricles was assessed using global longitudinal strain. The endpoint was in-hospital mortality. The mean age was 51.4 ± 18.3 years, and 54% were female. The average SOFA score at T0 was 8.6 ± 3.8 points and at day 7 was 4.9 ± 4.7 points. The left ventricular (LV) ejection fraction at baseline was 65.6 ± 9.1%, without changes in echocardiographic parameters during treatment. LV and RV longitudinal strain increased significantly in the patients who survived (- 18.8 ± 3.6 at D1 vs - 20.8 ± 2.5 at D7; p = 0.003; and - 21.3 ± 4.9 at D1 vs - 24.3 ± 5.8 at D7; p = 0.035, respectively), whereas strain values remained unchanged in those who died. After adjustment for the SOFA score, RV longitudinal strain at admission was associated with in-hospital mortality [adjusted odds ratio (OR) 0.760; 95% confidence interval (CI) 0.591-0.977; p - 0.033]. STE improved significantly after the first week of treatment in patients with sepsis who survived compared with those patients who died during hospitalization. RV strain at admission predicted in-hospital mortality. An improvement in STE during sepsis treatment appears to be a useful tool for predicting in-hospital outcome.

Cell-derived microvesicles in infective endocarditis: Role in diagnosis and potential for risk stratification at hospital admission.

OBJECTIVES: To characterize the plasmatic profile of cell-derived microvesicles (MVs) at diagnosis and during the treatment of patients with infective endocarditis (IE). METHODS: Blood samples from 57 patients with IE were obtained on 3 consecutive moments: upon admission (T0), at 2 weeks (T1), and at the end of treatment (T2), and were compared with 22 patients with other bacterial infections. MPs were measured by flow cytometry and labeled for specific cell markers of CD45 (leukocytes), CD66b (neutrophils), CD14 (monocytes), CD41a (platelets), CD51 (endothelial cells), CD3 (T lymphocyte) and CD235a (erythrocytes). RESULTS: MVs from platelets (pltMVs), leukocytes (leukMVs), neutrophils (neutMVs), monocytes (monoMVs) and lymphocytes (lymphMVs) were significantly more elevated in the patients with IE, compared to the patients with other bacterial infections, despite comparable age, sex, blood counts and C-reactive protein levels. MVs values revealed a relatively stable pattern over time in IE, except for a significant increase in leukMVs and neutMVs in T1. LeukMVs (p = 0.011), neutMVs (p = 0.010), monoMVs (p = 0.016) and lymphMVs (p = 0.020), measured at admission, were significantly higher in IE patients that died during hospitalization in comparison with those that survived. In a multivariable analyses, the levels of neutMVs remained as an independent factor associated with mortality (odds ratio 2.203; 95% confidence interval 1.217 - 3.988; p = 0.009), adjustment for heart failure during the treatment. CONCLUSIONS: Plasma levels of pltMVs, leukMVs, neutMVs, monoMVs and lymphMVs were significantly more elevated in patients with IE than in patients with other bacterial infections at hospital admission. Furthermore, neutMVs at admission have been identified as an independent predictor of mortality in patients with IE. Thus, cell derived MPs may become an important tool in the differential diagnosis and mortality risk assessment early in the course of IE suspected cases.